Dizziness and imbalance

Dizziness and imbalanceIn France, dizziness subject 300 000 visits per week, more than 15 million visits per year. From the outset, we note that the term “vertigo” is still often used by patients to describe discomfort. Dizziness, derived from Latinvertere turn, corresponds to the situation where the subject sees all turn to him. In our practice, “rotary” vertigo remains a tautology comfortable for a spot of vertigo species among others, for which “it does not really running,” the patient describing such a linear displacement sensation, “a linear vertigo “as if it slid sideways, fell or bowed. So we prefer to speak of “dizziness” in those cases where the patient may have a fleeting impression, uncertain that “it turns” before him. Beyond this accuracy, we must make a habit of distinguishing vertigo imbalance, ataxia walking, of standing become difficult station, and also distinguish the real imbalance in the simple sensation of instability or insecurity (no real loss of balance).

It is possible to identify 150 dizziness or imbalance typed, among which dominate three etiologies: paroxysmal positional vertigo Benin, Meniere’s disease and vestibular neuritis. Their pathophysiology are radically different and specifically adapted therapeutic.


Vestibular apparatus:

This specialized body in estimating the position of the head in space and in the detection of movement allows the central nervous system to respond through adaptation of the visual axis and posture, or by anticipation on movement to run.

The posterior labyrinth, located in the inner ear, has acceleration sensors formed by three semicircular canals measuring the angular accelerations in all three planes of Euclidean space, and a system otolith (utricle and saccule) measuring linear accelerations in all directions of space. Through the internal auditory canal, the afferent fibers of the vestibular nerve connecting the labyrinth with vestibular nuclei bulbar complex.

The vestibular nuclei are under control of the crosslinked, of tubéromammillaires nuclei of the cerebellum and vestibular cortex.

Effector connections are threefold:

– To the oculomotor nuclei by the medial longitudinal fasciculus (to stabilize the eyes);

– To the anterior horns of the spinal cord by the vestibulospinal beam (to adjust muscle tone according to the gravity and movement);

– To the nucleus of the vagus nerve (to control autonomic functions).

Visual system:

The visual system continuously estimates the linear displacements of the visual world and projects the motion information on the vestibular nuclei by the optical accessory pathway.

Proprioceptive system:

This system realizes muscle tension and movement performed by the body during the active or passive movements.We now know that it is in the whole musculature and not only in the muscles of the neck. Skin exteroceptive information, joint and visceral also come into play.

These three types of information – vestibular, visual and proprioceptive – let us know if it is we who move, the environment or both, but how fast and in which direction.

This explains for example that injured vestibular system works asymmetrically, and that this asymmetry is perceived as a movement. This in turn leads to an abnormal eye movement – a pathological nystagmus -, and an abnormal movement of the body – a deviation index, or deflection Romberg.

Dizziness or imbalance:

By origin, dizziness and imbalance differ priori.

It seems that the rotatory vertigo almost always reflects a sharp and sudden unilateral impairment of the vestibular system, often peripheral semicircular canals, rarely central vestibular system (vestibular nuclei and cerebellum bulbar).

For their part, the imbalances are primarily three possible causes:

– Progressive damage to the peripheral or central vestibular system (acoustic neuroma, reached the vestibular nuclei or cerebellum, minimal intrusion of the semicircular canals or central systems, bilateral involvement – ototoxic damage for example – or reached the otolith system );

– Impairment of proprioception extraocular muscles or antigravity muscles, including those of the neck;

– Multi-sensory impairment, especially in the elderly.


Often positional, vertigo this very brief (seconds to a minute) and paroxysmal moves like a wave, with latency and maximum (the peak). It alone accounts for 34% of dizziness and imbalance, or over a dizzying three, and affects one in twenty. This is true positional vertigo Benin vertigo (BPPV).

Sometimes vertigo is accompanied by tinnitus, deafness, one ear fullness. This is the classic Meniere disease, with many differential diagnoses too often referred to as “syndromes meniériformes”.

In front of a great rotatory vertigo that lasts for days, it must evoke primarily vestibular neuritis. This diagnosis, not always known general practitioners, deserves our attention because it requires very different drug treatment to those of Meniere’s disease, which now adds a balance training.

The shape type of imbalance is the central achievement.

Faced with a fear of losing balance, we must think of acrophobia (fear of heights).



The questioning of the patient with vertigo, as always in medicine, the key moment in the diagnostic process. Briefly, the patient will immediately guided to a specific type of dizziness or imbalance.

This examination can be conducted in different ways depending on the patient, however, must be rigorous. It necessarily includes certain questions whose answers are critical to the diagnostic process.

What happened to you?

The doctor let the patient tell his story, the directing sometimes with some specific questions to see if there is a giddiness or not: “Is it good for vertigo? Are we left quite agree on the words? Is it really turns? Is this the part that rotates or you? Or is it a lack of stability? Do you actually loss of balance, or is it just a sensation of instability? Are you afraid of falling?

Must be obtained from the patient clear answers to whether there is dizziness or imbalance, of a reality or fears.

Once installed it is a dizziness, instability or a feeling of imbalance, the doctor did specify certain crucial information from the patient to guide diagnostic evaluation. This examination is structured around three critical and essential concepts: duration, triggering circumstances and accompanying signs.

What is the duration of vertigo?

“… In seconds, minutes, hours, days? Is this the first time in your life? Is it a single dizziness or vertigo that is repeated?

Similar or not? What is the date of the early troubles? “We must try to get dates and specific times for each dizzying episode.

Are there triggering circumstances?

“… Particular positions of the head or body? Are there times or particular places: in or out, in bed, you are covered by car on the highway … “It should also inquire about the possible medications (antihypertensives, anxiolytics , neuroleptics).

Did you notice accompanying signs?

“… Tinnitus, hearing loss or ear full of sensation? Headache?

Nausea or vomiting (which indicate above all the intensity of dizziness)? Tachycardia, sweating, visual disturbances or tremors? And recent acute neck pain? “We must establish as complete a picture as possible of the events associated with dizziness.

Physical examination:

Some instruments such as an examination couch, otoscope, a tuning fork and a pair of Frenzel glasses are useful for examining a patient in acute vertigo attack. A dozen clinical skills to perform essential form the basis of this diagnostic purposes examination.

Systematic review of unscrambling:


The first step is to check the ear canals and eardrums two.


Using a pitch of 500 Hz, hearing is tested. The sound of the tuning fork is heard by the practitioner, then immediately placed close to each patient’s ears, who is asked if he understood, then it means a better side. We take advantage of the natural amortization of the intensity of the sound of the fork to test the patient’s hearing threshold. The foot of the vibrating tuning fork is placed on the bone behind the ear relief, mastoid, to hear the bone conduction patient, thus bypassing the tympanoossicular chain of the middle ear. Normally less mean bone conduction by air (eardrum and ossicles): If the patient hears better bone conduction is that deafness is located in the middle ear. The foot of the vibrating tuning fork is then placed on the bridge of the nose. The sound can be lateralized in one ear in the better ear in cases of sensorineural hearing loss and damage to the cochlea or the nerve, in the most deaf ear in case of conductive hearing loss.

At this point, the continued clinical review is to look for signs for authenticating dizziness and diagnostic signs: signs for a peripheral disorder – BPPV, unilateral vestibular cit recent challenge – and signs in favor of a central reached.

Benin paroxysmal positional vertigo:

Faced with a dizzying patient should be performed systematically diagnostic Hallpike maneuver: the subject is sitting in the middle of the examination couch, legs dangling. A hand on a patient’s neck, the other hooking his arm, the practitioner layer the patient in the lateral position, head turned 30 ° relative to the horizontal.

Under Frenzel glasses or direct examination, there is possible occurrence of a contemporary vertigo nystagmus. the direction of nystagmus is specified, its climax, its duration (see Fig. 1 and 2 in chapter fi n).

The subject is then rectified. We appreciate if nystagmus reappears, synchronous or not with a vertigo, and there is its direction. The subject is then coated on the other side, by a symmetrical maneuver, which may in turn trigger a rotatory vertigo accompanied nystagmus geotropic (rolling down), occurring after a latency of 1 to 2 seconds and during 10 to 20 seconds. The return to sitting still causes vertigo and rotatory nystagmus whose meaning is reversed. This is typical of a Benin paroxysmal positional vertigo due to a mechanical disorder of the inner ear.

In the case of a central positional nystagmus, dizziness are very low or absent.

Nystagmus appears as soon as the patient is put into the triggering position, and has two features: it persists as long as the position and it is not inhibited by visual fixation.

Recent unilateral vestibular deficit:

Review of vestibulospinale function:

This review includes five stages, the first consisting of the mere observation of the progress of the patient as it enters the cabinet.

* Romberg Test:

It is to study the posture of a standing subject,

feet, at attention and you eyes closed. Normally you do not notice any oscillation. A tendency to fall to one side – the pathological side – and only if this is repeated lateralization, evokes a peripheral deficit syndrome, while large non systematized oscillations rather evoke a central pathology.

* Test the blind march:

The patient is asked to close his eyes, to move three to five steps, then back to even. We appreciate the sense of the deviations.

Deviant permanently to the deficit side, the patient with peripheral pathology draws on his march, a star.

* Test the blind trampling (Fukuda test or test of Unterberger):

The subject is asked to mark time at the rate of one step per second, raising the knee about 45 ° and keeping the arms stretched forward. Again, we appreciate especially the rotations there.

* Reactions to the postural brief push:

It is located behind the subject – previously warned – in Romberg position: is carried out with both hands a brief traction on its two shoulders back and observed its reaction.

Normally, dodge postural response is to make a small step back to block the fall and / or lean forward.

If defi cit, the share patient back on his heels, sometimes losing his balance as to fall if not held him back.

Search nystagmus:

Nystagmus is an involuntary movement and rhythmic back and forth synchronously in both eyes.

It includes a slow phase and a quick return, two phases (or shaking) of elementary opposite directions. One can observe all axes: horizontal nystagmus, vertical or torsional.

By convention, the direction of the fast twitch defines the direction of nystagmus: left, right, up, down.

* Some generalities:

In simple examination, it is easier to mark nystagmus by asking the patient to look at a plain wall or ceiling, because the lack of visual cues increases intensity. eye is observed in a focused gaze, then in a laterally offset relation to 20 ° to 30 ° (we always avoid offset look beyond 40 °, for then appears a physiological point of nystagmus.)

* The Head shaking nystagmus:

This is nystagmus revealed by the shaking of the head. This awareness maneuver is performed by rapidly shaking the subject’s head in the horizontal plane, then he is asked to look straight ahead a large flat surface.

Central reached:

Detection of a “gaze nystagmus”:

The subject is asked to watch a test pattern (a colored dot on a pen) in the opposite side, then in the left eye 30 or 40 centimeters, then at 20 ° and 30 ° eccentricity; same right, up, and down. In normal subjects, it is only possible from 40 ° eccentricity appears physiological nystagmus. However, the onset of nystagmus from 20 ° eccentricity left in the gaze to the left, or right in the eye right or upper vertical gaze in the top or bottom vertical in the look down, reveals generally, if both eyes fight with equal amplitude (if the nystagmus is congruent), cerebellar pathology. this is called a “nystagmus gaze.”

If the nystagmus is further on the eye in abduction or exists only on the eye in abduction, this is a monocular nystagmus ataxic Harris that evokes a brainstem lesion, specifically a lesion of ‘interneuron (between the nucleus and the VI kernel III) and can be part of a internuclear ophthalmology.

Test for eye tracking:

the precise point of the tip of a pen with which performs sinusoidal movements back and forth in the horizontal plane one takes 60 centimeters of the subject who is asked to follow. Examines his eyes as he follows this movement.Normally, the prosecution is flexible, regular, smoothly without jerking. Sometimes, there jerks that evoke a cerebellar syndrome, or occipital or parietal involvement.

Locating a vertical nystagmus:

Vertical nystagmus, beating up or down and visible in the eyes of the face is typical of central origin, often following a lesion of the brainstem or cerebellar lesion (anterior).

Detection of an infringement of verticality:

If a violation of the vertical eye movements upwards and / or downwards or even vertical or oblique diplopia are highlighted, it can be a skew deviation. The lesion may be in the vestibular nuclei in the medulla (Wallenberg). In this case, the eye ipsilateral to the lesion is typically lower than the other. In the case where the lesion resides stem floor, the ipsilateral eye to the lesion is typically higher than the other.

Verifying removal of vestibular nystagmus by visual fixation:

The subject is asked to stand up, elbows close to the body to hold onto a pen in front of him at about 40 centimeters from his eyes, and watch carefully the colored end of the pen. the patient is rotated a rotation left-right alternating movement of about 30 ° amplitude. During this stimulation, inhibits its normal subjects nystagmus with visual fixation.

Exploration of other cranial nerves, particularly V and VII:

We must not omit in the search for signs of a central achievement explore other cranial nerves, especially V and VII.

Finish with the patient’s general examination:

It is useful at the end of this clinical examination for signs in favor of a central achievement to end with a general examination of the patient.

Specialized Additional tests:

When, why and how to explore a dizzy? When taking and clinical examination are not clear.

Because the signs are sometimes misleading, and the patient may present atypical forms.

These examinations are performed by the ENT specialist or neurologist.

Caloric test:

The caloric test is a key test of the vestibular exam, although it is usually performed last because it can cause nausea might interfere with the results of the following tests. It assumes the tympanic integrity: for patients whose eardrum is damaged, the stimulus is produced by air and not water.

The patient is lying, trunk statement of 30 °, which puts the system on external semicircular canals upright. one vestibule is studied both: the irrigation of the external auditory canal by water whose temperature is higher (44 °) or less (30 °) than the body causes a warming or cooling labyrinthine liquids become the seat of exciting thermal convection or inhibiting buccal cells of the crest of the external semicircular canal. In normal subjects, hot irrigation is exciting and causes nystagmus beating toward the ear stimulated nystagmus right for a hot stimulation of the right ear, while inhibiting cold irrigation and causes nystagmus beating side opposite to the ear stimulated nystagmus left to cold stimulation of the right ear.

Vidéonystagmographique review:

The vidéonystagmographique examination (VNG) miniaturized infrared video cameras recorded the spontaneous nystagmus and nystagmus caused by caloric tests


Audiometry tests for each ear, the auditory pathway as a whole.


The impedance explores the middle ear (ossicles and Eustachian tube).


auditory evoked potentials (AEP) brainstem allow a focus on the activity of the first centimeters of the auditory pathways, ie the typical location of acoustic neuroma, a real obsession ENT.

To scan :

The scanner provides images of labyrinthine hull.

Centered on the inner ear, it serves primarily to see translabyrinthine fractures and argues for the diagnosis of otosclerosis.


MRI studies primarily the nervous system: the nerve cochleovestibular, cerebellopontine angle and the posterior fossa.To optimize the diagnostic process in general and the record of these images difficult to interpret, in particular, avoid prescription with additional examinations blindly, and explain to the radiologist what you want.


To talk, listen, require precise terms, durations and combinations of symptoms: a methodical examination often provides all the necessary elements to diagnosis.

This is what we show now proposing, closer symptoms, a study in six tables.

And positional vertigo brief:

Benin paroxysmal positional vertigo:

We have seen that BPPV is by far vertigo

The most frequent (one third of cases of dizziness and imbalance). Long misunderstood and mistaken for cervical or vertebrobasilar disease, BPPV is due to an otolith movement in the semicircular canals of the inner ear. A therapeutic maneuver reversal of the inner ear is often effective immediately. This means the interest for the patient early diagnosis and judicious treatment.


The description by the patient during the interrogation immediately brings to mind the diagnosis: typically, the patient described a very brief few seconds dizziness, occurring in very specific triggering circumstances: in turning in bed or turning the head but also rising, stooping, putting upside extension. Apart from these triggers movements, it feels nothing, or instability that improves during the day.

All forms are possible, since the single dizzy for a split second when turning the head to the crises, repeating the slightest movement of the head for several tens of minutes, prevent the patient to leave the position inhibiting dizziness. We note the absence of headache, hearing loss, tinnitus and phosphene: at best patient he described a very busy feeling of heaviness in the head. Number of BPPV occurs after a brain injury, even minor, or a whiplash.

Physical examination:

If there is indeed a BPPV, diagnostic maneuver Hallpike reproduces the vertigo accompanied rotatory nystagmus geotropic characteristic (Fig. 1 and 2).

Note that there is no place in the presence of a paroxysmal positional vertigo Benin with a positive Hallpike maneuver, to practice or to request additional investigations; as there is no place to practice or apply in case of isolated vertigo, an electroencephalogram (EEG) or a Doppler ultrasound.


The main treatment for BPPV is the therapeutic maneuver: the patient is placed in a position of Hallpike the affected side (Fig. 2).

After stopping the vertigo and nystagmus, the doctor realize the patient a flop of 180 ° (Fig. 3). The patient is left on the side or stomach, head 45 ° to the ground.

He feels, after a delay of several seconds to several minutes, an intense but brief dizziness and the doctor observes a rotatory nystagmus.

These events are witnessed an output of otolith semicircular canal. In 80% of cases, the patient is immediately cured;otherwise, the operation is repeated. No drug treatment has proved effective in this type of vertigo. An antiemetic can sometimes be effective in cases of nausea and vomiting, as well as an anxiolytic.

The presentation of BPPV would not be complete without its differential diagnoses, four in number: postural hypotension, vertebrobasilar insufficiency, cervical pathology or a central achievement.

Orthostatic hypotension:

This dizziness is extremely common. We find, during the interrogation, decisive information: it is only when it rises suddenly or looks up the patient to experience malaise accompanied by some phosphenes and sometimes dysesthesia disappearing in seconds. Taking tension in prone and standing position brings the key to diagnosis. The fall in blood pressure must appear in the first five minutes of orthostatic. This type of vertigo accompanied not normally nystagmus.

Vertebrobasilar insufficiency:

Long regarded as a major cause of vertigo, it is actually rare and represents less than 1% of our consultations dizziness. During examination, the doctor found brief dizzy for a few seconds to minutes. If they are associated with visual events such qu’obscurcissement or tunnel vision, or with headache or other typically neurological symptoms, the doctor may suggest a vertebrobasilar insufficiency.

Cervical Pathology:

Some patients with cervical functional disorders experience dizziness.

Most often, it is simple sensations of imbalance. The etiology is often disputed.

Central reached:

Headache, nystagmus gauze, eye tracking, hypermétries eye saccades, ocular fixation test and vertical nystagmus are all clinical arguments that evoke the happily rare cause.

Great crises of repetitive dizziness:

Meniere’s Disease:

The mistake not to commit, especially during the first crisis, is to link the patient’s symptomatology to a digestive pathology examination can recognize vestibular symptomatology.

Figure 1. Diagnostic Hallpike Maneuver, starting position
Figure 1. Diagnostic Hallpike Maneuver, starting position


The vertiginous access generally last between fifteen minutes and several hours, then subside gradually. The patient reveals the typical accompanying signs: the crisis often begins with an ear fullness printing, unilateral serious buzz, conventionally “conch.”

Nausea and vomiting often occur at the peak of the crisis and relieve the patient but often mislead diagnosis towards an “upset stomach”. In many patients, the crisis persists after acute tinnitus.

The evolution of the disease shows that after each crisis hearing loss, typically affecting the lower frequencies, worsening a little more.

After several years, deafness is important and the great vertiginous crises give way to an almost permanent instability.

Physical examination:

Figure 2. Diagnostic Hallpike maneuver, revealing Benin positional vertigo (BPPV) left
Figure 2. Diagnostic Hallpike maneuver, revealing Benin positional vertigo (BPPV) left

A patient with these symptoms should be referred to an ENT to confirm the diagnosis.

The waning of the crisis, he practices an audiometric assessment, auditory evoked potentials, a test to glycerol, a videonystagmography and vestibular caloric tests.

Differential diagnosis:

Four conditions are mentioned: otosclerosis, chronic otitis – with or without cholesteatoma – the labyrinthine fistula and acoustic neuroma (which must now appoint vestibular schwannoma).


Treatment is based on betahistine hydrochloride (Betaserc® 24 and its many generic): 3 tablets of 8 mg morning and evening for dinner, a little salt-free diet and a healthy lifestyle. There is often a psychosomatic component rather difficult to handle.

Figure 3. Left therapeutic maneuver for BPPV
Figure 3. Left therapeutic maneuver for BPPV

Large single vertigo crisis during several days:

Vestibular neuritis:

Patients with vestibular neuritis of great brutally isolated vertigo that lasts for hours or even days. The examination found neither concept of hearing loss or tinnitus, nor any particular past otologic or headaches or specific neurological signs. The evolution is towards instability that will yield a few weeks.

Confirmation of the diagnosis is provided by the caloric test that reveals the challenge cit unilateral acute labyrinthine as uncompensated vestibular loss.

As herpes zoster, chickenpox or mumps, vestibular neuronitis is typically a viral infection by a neurotropic virus.

Adding that the balance sheet must always include audiometric testing and auditory evoked potentials to remove a neuroma VIII or central involvement.

Head trauma with fracture of rock:

We find here also a great rotatory vertigo crisis which regresses within weeks.

But the questioning allows to add to it the notion of trauma accompanied possibly otorragies, facial palsy, deafness.

The objective caloric vestibular exam the uncompensated unilateral deficit and balance the scanner finds the fracture.

Ischemic stroke in the brainstem or cerebellum:

The classic and typical form is Wallenberg syndrome characterized by a rotatory vertigo for several days or weeks.

The examination may reveal, among the accompanying signs, the presence of headache, hiccups, but also dysphonia.

Associated with the clinical examination, vestibular testing and caloric oculographiques show, in addition to the challenge cit labyrinthine signs of central achievement – Eye lateropulsion, “gauze nystagmus” saccadic prosecution abnormal fixation index.

The neurological examination showed ipsilateral cerebellar syndrome, a syndrome ipsilateral Horner, facial anesthesia dissociated affecting heat and tenderness, ipsilateral paralysis hémivoile, the hémipharynx and vocal cord, finally hemianaesthesia a member of the body type dissociated contralateral to the lesion.

Imaging the extent of the damage.

This is a medical emergency that often require intubation and patient hospitalization in neurosurgical intensive care.This is, in our view, the only real emergency in acute dizziness.

Isolated instability without other neurological:

In these patients never having, or substantially all of rotatory sensations, the complaint concerns a permanent or transient instability that hinders them in their daily lives. Again, the examination is often enough to establish the diagnosis.

Otolith syndrome:

Such a patient for example tells how, as he walked, he felt inexorably drawn to one side, perceiving itself obliquely to the vertical; while another said he had the sensation that his head is closer to the ground as “shifted”.

Many symptoms are related to the sensations perceived by car: such a patient described that he felt his head continue moving forward during a sudden brake at a red light; another such that, tight turns, his body (or his car) took the tangent of the turn, or he mistakenly believed that his car was bent as if two tires were deflated on one side.Sometimes it’s in the elevator that the patient felt that the cabin movement continued after stopping.

Acoustic neuroma:

We must have this condition in mind as it manifests itself only rarely by large vertiginous crises. The instability phenomena occur late. The patient reveals that he makes when walking swerving, it is unbalanced in the dark.

But it is above all to the presence of a progressive unilateral deafness with or without tinnitus, to think it. The vestibular examination, showing a unilateral offset defi cit is imperative completed by audiometry, auditory evoked potentials and imaging (CT, MRI).

Reached by ototoxic:

It can be a challenge cit bilateral vestibular device by ototoxic damage – especially by aminosidiques antibiotic gentamicin kind. The main complaint of the patient wears on ataxia increased by darkness (if he gets up at night, or when he closed eyes), but it can also suffer from hearing loss.

The vidéonystagmographique examination revealed bilateral vestibular loss to commuters caloric and rotational tests, allowing the differential diagnosis with a central achievement. Clinical examination and objective Posturographic ataxia. As for the audiometric test, it allows the monitoring of hearing thresholds.

Hypoglycemia, anemia, polycythemia, respiratory failure:

A measure of the oxygen saturation finger (SaO2), blood count, and blood glucose (or a glucose tolerance orally) will identify these pathologies.

Visual source of instability:

The patient complains of being unstable when high or when optokinetic stimulations (when looking to start a train when he sees a parade of white lines on the floor in the car, etc.).


The presbyataxie concerns of the elderly in whom the different functions contributing to the equilibration are disturbed: visual problems, presbyvestibulie and deep sensitivity disorders. The patient complains of a multitude of small disorders who “spoil life”: he sees less, works less well, may fall and is afraid to go out. All this involved the imbalance in the elderly, falls source of known, alas, frequent consequences – hip fracture, dependence, etc.

Instability with other neurological signs:

Multiple sclerosis:

In young people, MS is frequently manifested by disorders of balance. The interrogation research in history the existence of extensive self-limiting: paresthesia, electrical shooting pains, facial neuralgia, oculomotor disturbances.

The vidéonystagmographique review, with study of eye movements by video oculography, often shows an internuclear ophthalmoplegia, and cerebellar syndrome. In advanced cases, optic neuritis retrobulbar is almost constant. It is evidenced by visual evoked potentials showing a wave latency prolongation P 100. The MRI can detect the presence of hyperintensity often revealing subclinical lesions.

Parkinson disease:

This is the most common extrapyramidal syndromes.

Parkinsonism combines classically akinesia, hypertonia and tremor, and is responsible for many gait, imbalance and falls. It is sometimes the consequence of neuroleptic treatment or neuroleptic less known component of an anti-vertigo – Torecan®, Sibelium®, Stugeron® – or antiemetic – Primperan® – often prescribed too long.

Syndrome Steele-Richardson-Olszewski or progressive supranuclear ophthalmoplegia:

This other extrapyramidal syndrome not responding to conventional treatment that is dopamine, and its evolution is more serious. Often the disease begins with balance disorders, unexpected falls, a trend retropulsion and gait disturbance. Added to cerebellar signs and central disorders. The first relates ophtalmoplegia verticality and horizontality, and is primarily reflected in a slowdown of saccadic eye movements. Dysarthria and swallowing disorders are also observed.

Normal pressure hydrocephalus:

This disorder often affecting the elderly is recognized by gait disorders associated with sphincter disorders and intellectual deterioration. Initially, the patient complains of instability, lightheadedness walking, difficulty climbing stairs.Later, walking is slow, cautious and takes place in small shuffling steps. superior functions disorders associate, resulting in a reduction of activities and a certain disinterest. The scanner shows an expansion of the ventricular system.

Incomplete state occurring in a hypertensive patient:

Gaps in the hypertensive subject are often low noise. In most cases, symptoms which resolved quickly: it may be of little fainting, dysarthria, of hémiparesthésie or balance disorders.

Over time, balance disorders become more frequent, more painful and the patient walks with small steps: a true impotence can develop.

sphincter control disorders are sometimes added to the pseudobulbar state. Sometimes even this incomplete state progresses to dementia.

Cerebellar atrophy:

We meet this condition or as part of a chronic alcoholism or in that of a hérédodégénérescence spinocerebellar – like Friedreich’s ataxia – which combines a cerebellar syndrome in a pyramidal syndrome and posterior radiculocordonal syndrome. The patient has a widening of support polygon with lightheadedness walk, while radiculocordonal syndrome gives talonnante walk with hypotonia. The later pyramidal syndrome causes a motor deficit. The clinical examination is characterized by a hollow foot and kyphoscoliosis which exacerbates the gait.

Peripheral neuropathy:

Whether they are diabetic, alcoholic or drug to deficiency or sometimes, these disorders cause balance problems with muscle weakness and falls.

The abolition of the Achilles tendon and knee jerks did suggest the diagnosis. It’s electromyographic examination confirms this.

Brain tumors:

The practice of brain imaging (CT or MRI) allows not to disregard them.

Cervical spondylotic myelopathy and Chiari malformations:

Again it is the imaging of the cervical spine and atlanto-occipital hinge which will track.

Instability feeling no real instability:


The examination shows that this isolated instability occurs in well-defined circumstances, namely crowded places, open spaces, restaurants or department stores, etc. There is no ataxia clinical examination without triggering locations.

Panic Attack:

Suddenly, the patient can not move forward, he knows more out of this unexpected ambush: down an escalator, out of this crowd, go into a store or simply go his way. He may feel that the ground will open beneath his feet.

Phobic postural syndrome:

The patient doubts his performance. He walks not careful, sometimes dragging their feet as if walking on ice. If given the hand, even symbolically a finger, everything falls into place.

Vestibular Syndrome negligence:

The patient no longer reflects his vestibular information, and everything moving around makes him dizzy, and could disturb the drop down. In the vestibular exam, its arches are operating normally.

Proprioceptive disorders (especially in the nuchal region):

Proprioceptive disorders cause the minimal balance disorders that can be improved by rehabilitation.


It is a diagnosis of exclusion, to remember with caution, and after practicing a brain imaging.


It is the man who puts on the track when one finds a triggering event, sleep disorders, unexplained fatigue.


The main merit of focusing on the questioning of the vertiginous patient probably lies in the awareness that this time of the consultation is crucial in many respects.

First of all because the doctor draws the essentials of diagnosis: type of vertigo or imbalance, duration, intensity, associated signs.

Based on clinical examination and additional examinations (videonystagmography, audiometry and possibly auditory evoked potentials), it can confirm the diagnosis before proposing appropriate treatment.

And then because some patient complaints, formerly ignored or interpreted as psychosomatic, are now recognized as authentic vestibular manifestations, sometimes otolithic: we now know that about 20% of chronic and recurrent vestibular disorders are followed by disorders such as agoraphobia, panic attacks, phobic postural syndrome or negligence vestibular syndrome.